Adams J M, Feustel P J, Donnelly D F, Dutton R E
Adv Shock Res. 1978;1:209-20.
During hemorrhagic shock, increased uptake of NH3 from the gut with inadequate compensation by the liver results in hyperammonemia. The effect on brain metabolism of acute hyperammonemia alone, as compared with normocapnic hypoxia, was investigated in 11 pentobarbital anesthetized (30 mg/kg) dogs. These animals were paralyzed (pancuronium bromide) and artificially ventilated to maintain the end-tidal fraction of FETCO2) CO2 constant. Arterial blood and cerebrospinal fluid (CSF) samples were obtained following control, 30-minute hypoxia, 60-minute NH3 infusion, and 30-minute hypoxia combined with NH3 infusion. These were analyzed for PaO2, PCO2, pH, and NH3. CSF samples were further analyzed for glutamine, urea, lactate, pyruvate, and citrate. There were no significant changes in urea or citrate. Glutamine, lactate, and the lactate/pyruvate ratio were significantly elevated by hypoxia and by NH3 infusion. (formula: see text). Thus, an acute NH3 load is capable of disrupting aerobic glycolytic metabolism. Hence, hyperammonemia may affect brain function during shock.
在失血性休克期间，肠道对氨的摄取增加，而肝脏的代偿不足，导致高氨血症。在11只戊巴比妥麻醉（30毫克/千克）的狗身上，研究了单纯急性高氨血症对脑代谢的影响，并与正常碳酸血症性缺氧进行了比较。这些动物被麻痹（泮库溴铵）并进行人工通气，以维持呼气末二氧化碳分数（FETCO2）恒定。在对照、30分钟缺氧、60分钟氨输注以及30分钟缺氧联合氨输注后，采集动脉血和脑脊液（CSF）样本。对这些样本进行动脉血氧分压（PaO2）、二氧化碳分压（PCO2）、pH值和氨的分析。脑脊液样本进一步分析谷氨酰胺、尿素、乳酸、丙酮酸和柠檬酸。尿素或柠檬酸没有显著变化。缺氧和氨输注使谷氨酰胺、乳酸以及乳酸/丙酮酸比值显著升高。（公式：见正文）。因此，急性氨负荷能够破坏有氧糖酵解代谢。因此，高氨血症可能在休克期间影响脑功能。
